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Biphasic Dose Response in LLLT – An Update may cause cell damage, and then induce expression of anti-oxidant defenses such as superoxide dismutase and catalase. LLLT was reported to produce a shift in overall cell redox potential in the direction of greater oxidation (Karu 1999) and increased ROS gen- eration and cell redox activity have been demonstrated (Lubart et al. 2005). These cytosolic responses may in turn induce transcriptional changes. Several transcription factors are regulated by changes in cellular redox state, but the most important one is nuclear factor κB (NF-κB). Figure 1 graphically illustrates some of the intracellular signaling path- ways that are proposed to occur after LLLT. NO release and NO signaling There have been reports of the production and/or release of NO from cells after in vitro LLLT. It is possible that the delivery of low flu- ences of red/NIR light produces a small amount of NO from mitochon- dria by dissociation from intracellular stores (Shiva and Gladwin 2009), such as nitrosothiols (Borutaite et al. 2000), NO bound to hemoglobin or myoglobin (Lohr et al. 2009; Zhang et al. 2009) or by dissociation of NO from Cco (Lane 2006) as depicted in Figure 2. A second mechanism for FIG. 1. Schematic depiction of the cellular signaling pathways triggered by LLLT. After photons are absorbed by chromophores in the mitochondria, respiration and ATP is increased but in addition sig- naling molecules such as reactive oxygen species (ROS) and nitric oxide (NO) are also produced. 605PDF Image | BIPHASIC DOSE RESPONSE IN LOW LEVEL LIGHT THERAPY AN UPDATE
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